[Seawater exposure exacerbates scald burns-induced intestinal injury in rabbits: study of the mechanisms].
Pei Xu, Jiahan Wang, Pengwei Shi, Jun Ma
Abstract
Pei Xu, Jiahan Wang, Pengwei Shi, Jun Ma
Abstract
OBJECTIVE: To investigate the effect of seawater exposure on intestinal injury in rabbits with scald burns and explore the mechanisms. METHODS: Sixty-three rabbits with scald burns covering 20% total body surface area were randomized equally into scald control group (group A), scald with freshwater exposure group (group B), and scald with seawater exposure group (group C). At 2, 4 and 8 h after scald burns, 7 rabbits from each group were sacrificed for detecting plasma superoxide dismutase (SOD) and lipid peroxide (LPO) levels and intestinal contents of prostaglandins (PGs) and for examining the intestinal pathologies; immunohistochemistry was used to detect the expression of Bax and Bcl-2 proteins in the small intestinal epithelium. RESULTS: The rabbits in group C showed severer intestinal mucosal and barrier function damages than those in groups A and B. The plasma SOD activity and intestinal PGs contents were significantly lowered in group C than in groups A and B at 2, 4, and 8 h postburn (P<0.01) and reduced as the postburn time extended (P<0.01). In group C, plasma LPO content was the highest among the groups (P<0.01) and increased significantly with the seawater exposure time (P<0.01). The expression of Bax and Bcl-2 in the intestinal mucosal tissues was also the highest in group C (P<0.01) at 4 h and 8 h postburn and increased significantly with time (P<0.01). CONCLUSION: Seawater exposure exacerbates scald burn-induced intestinal mucosal and barrier function damages in rabbits mainly by aggravating intestinal inflammation and structural damage, as evidenced by decreased intestinal PGs contents and plasma SOD activity, increased plasma PLO content, and enhanced Bax and Bcl-2 protein expressions in the intestinal mucosa.
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OBJECTIVE: To investigate the effect of seawater exposure on intestinal injury in rabbits with scald burns and explore the mechanisms. METHODS: Sixty-three rabbits with scald burns covering 20% total body surface area were randomized equally into scald control group (group A), scald with freshwater exposure group (group B), and scald with seawater exposure group (group C). At 2, 4 and 8 h after scald burns, 7 rabbits from each group were sacrificed for detecting plasma superoxide dismutase (SOD) and lipid peroxide (LPO) levels and intestinal contents of prostaglandins (PGs) and for examining the intestinal pathologies; immunohistochemistry was used to detect the expression of Bax and Bcl-2 proteins in the small intestinal epithelium. RESULTS: The rabbits in group C showed severer intestinal mucosal and barrier function damages than those in groups A and B. The plasma SOD activity and intestinal PGs contents were significantly lowered in group C than in groups A and B at 2, 4, and 8 h postburn (P<0.01) and reduced as the postburn time extended (P<0.01). In group C, plasma LPO content was the highest among the groups (P<0.01) and increased significantly with the seawater exposure time (P<0.01). The expression of Bax and Bcl-2 in the intestinal mucosal tissues was also the highest in group C (P<0.01) at 4 h and 8 h postburn and increased significantly with time (P<0.01). CONCLUSION: Seawater exposure exacerbates scald burn-induced intestinal mucosal and barrier function damages in rabbits mainly by aggravating intestinal inflammation and structural damage, as evidenced by decreased intestinal PGs contents and plasma SOD activity, increased plasma PLO content, and enhanced Bax and Bcl-2 protein expressions in the intestinal mucosa.
Key concepts: Superoxide dismutase, Intestinal mucosa, Internal medicine, Barrier function, Chemistry, Intestinal epithelium, Ileum, Seawater